Plant Growth Inhibitory Activity and the Response of Different Rootstocks to Soil Sickness Syndrome in Japanese Pear Tree

Soil sickness syndrome in Japanese pear (Pyrus pyrifolia (Burm.f.) Nakai) affects the growth of the tree and decreases fruit yield. This study investigated the growth-inhibitory activity in Japanese pear (Pyrus pyrifolia (Burm.f.) Nakai) using the rhizosphere soil assay method to elucidate the characteristics of growth-inhibitory substances in Japanese pears. As a result, the root bark had the highest growth inhibitory activity during the growing season of the Japanese pear. For comparative analysis, the growth-inhibitory activities of Japanese apricots (Prunus mume Sieb. Et Zucc.) and figs (Ficus carica L.) were also investigated. Similar to the Japanese pear, the root bark of Japanese apricots and figs had a higher inhibition rate than the root pith. Like Japanese apricots and figs, it was inferred that the growth inhibitory substances accumulate in the bark of the Japanese pear. Furthermore, soil sickness syndrome in Japanese pear saplings did not occur when a fragment of Japanese pear shoots or thick roots was mixed with non-pear soil (soil with no history of Japanese pear cultivation). Based on these findings, it is considered that the condition of soil sickness in Japanese pear is caused by the accumulation of phenolic compounds such as arbutin, which is accumulated in the bark of the tree, secreted from the roots, and subsequently builds up in the soil. Additionally, the degree of occurrence of soil sickness syndrome depending on the rootstock was clarified. It was observed that the rate of growth inhibition was significantly higher in Pyrus betulifolia (Birchleaf pear) than in Pyrus pyrifolia (Japanese pear). Even when Japanese pear trees were planted in soils with no history of Japanese pear cultivation, the initial growth of P. betulifolia was 1.4 times that of P. pyrifolia. It is suggested that P. betulifolia is weak against soil sickness, but is excellent at initial growth itself. Our findings are important because P. pyrifolia is used for cultivation, in combination with other mitigation measures, such as soil dressing in replanted fields

Plant Growth Inhibitory Activity and the Response of Different Rootstocks to Soil Sickness Syndrome in Japanese Pear Tree

Soil sickness syndrome in Japanese pear (Pyrus pyrifolia (Burm.f.) Nakai) affects the growth of the tree and decreases fruit yield. This study investigated the growth-inhibitory activity in Japanese pear (Pyrus pyrifolia (Burm.f.) Nakai) using the rhizosphere soil assay method to elucidate the characteristics of growth-inhibitory substances in Japanese pears. As a result, the root bark had the highest growth inhibitory activity during the growing season of the Japanese pear. For comparative analysis, the growth-inhibitory activities of Japanese apricots (Prunus mume Sieb. Et Zucc.) and figs (Ficus carica L.) were also investigated. Similar to the Japanese pear, the root bark of Japanese apricots and figs had a higher inhibition rate than the root pith. Like Japanese apricots and figs, it was inferred that the growth inhibitory substances accumulate in the bark of the Japanese pear. Furthermore, soil sickness syndrome in Japanese pear saplings did not occur when a fragment of Japanese pear shoots or thick roots was mixed with non-pear soil (soil with no history of Japanese pear cultivation). Based on these findings, it is considered that the condition of soil sickness in Japanese pear is caused by the accumulation of phenolic compounds such as arbutin, which is accumulated in the bark of the tree, secreted from the roots, and subsequently builds up in the soil. Additionally, the degree of occurrence of soil sickness syndrome depending on the rootstock was clarified. It was observed that the rate of growth inhibition was significantly higher in Pyrus betulifolia (Birchleaf pear) than in Pyrus pyrifolia (Japanese pear). Even when Japanese pear trees were planted in soils with no history of Japanese pear cultivation, the initial growth of P. betulifolia was 1.4 times that of P. pyrifolia. It is suggested that P. betulifolia is weak against soil sickness, but is excellent at initial growth itself. Our findings are important because P. pyrifolia is used for cultivation, in combination with other mitigation measures, such as soil dressing in replanted fields

Gosha-jinki-gan (a Herbal Complex) Corrects Abnormal Insulin Signaling

Previous studies have shown that the traditional herbal complex Gosha-jinki-gan (GJG) improves diabetic neuropathy and insulin resistance. The present study was undertaken to elucidate the molecular mechanisms related with the long-term effects of GJG administration on insulin action in vivo and the early steps of insulin signaling in skeletal muscle in streptozotocin (STZ) diabetes. Rats were randomized into five subgroups: (1) saline treated control, (2) GJG treated control, (3) 2-unit insulin + saline treated diabetic, (4) saline + GJG treated diabetic and (5) 2-unit insulin + GJG treated diabetic groups. After seven days of treatment, euglycemic clamp experiment at an insulin infusion rate of 6 mU/kg/min was performed in overnight fasted rats. Despite the 2-unit insulin treatment, the metabolic clearance rates of glucose (MCR, ml/kg/min) in diabetic rats were significantly lower compared with the controls (11.4 ± 1.0 vs 44.1 ± 1.5; P < 0.001), and were significantly improved by insulin combined with GJG or GJG alone (26 ± 3.2 and 24.6 ± 2.2, P < 0.01, respectively). The increased insulin receptor (IR)-β protein content in skeletal muscle of diabetic rats was not affected by insulin combined with GJG administration. However, the decreased insulin receptor substrate-1 (IRS-1) protein content was significantly improved by treatment with GJG. Additionally, the increased tyrosine phosphorylation levels of IR-β and IRS-1 were significantly inhibited in insulin combined with GJG treated diabetes. The present results suggest that the improvement of the impaired insulin sensitivity in STZ-diabetic rats by administration of GJG may be due, at least in part, to correction in the abnormal early steps of insulin signaling in skeletal muscle